This third edition of what has now become a well-established textbook in cardiovascular medicine is again edited by Dr Eugene Braunwald with the assistance of 65 other authors who read like a Who's Who of American Cardiology. Since the second edition, 12 new chapters have been added or substituted and others have been significantly revised. The first volume includes Part I on "Examination of the Patient" and Part II on "Normal and Abnormal Circulatory Function." The second volume deals with specific diseases. Part III, "Diseases of the Heart, Pericardium and Vascular System," includes new sections on "Risk Factors for Coronary Artery Disease," "The Pathogenesis of Atherosclerosis," and "Interventional Catheterization Techniques." Part IV, "Broader Perspectives on Heart Disease and Cardiologic Practice," includes new chapters on "Genetics and Cardiovascular Disease," "Aging in Cardiac Disease," and "Cost Effective Strategies in Cardiology." The last 200 pages of the book (Part V) are devoted to

Heart Disease: A Textbook of Cardiovascular Medicine

The "2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care" increased the focus on methods to ensure that high-quality cardiopulmonary resus...

Cardiopulmonary resuscitation quality: Improving cardiac resuscitation outcomes both inside and outside the hospital: A consensus statement from the American heart association

Liver cirrhosis is the final pathological result of various chronic liver diseases, and fibrosis is the precursor of cirrhosis. Many types of cells, cytokines and miRNAs are involved in the initiation and progression of liver fibrosis and cirrhosis. Activation of hepatic stellate cells (HSCs) is a pivotal event in fibrosis. Defenestration and capillarization of liver sinusoidal endothelial cells are major contributing factors to hepatic dysfunction in liver cirrhosis. Activated Kupffer cells destroy hepatocytes and stimulate the activation of HSCs. Repeated cycles of apoptosis and regeneration of hepatocytes contribute to pathogenesis of cirrhosis. At the molecular level, many cytokines are involved in mediation of signaling pathways that regulate activation of HSCs and fibrogenesis. Recently, miRNAs as a post-transcriptional regulator have been found to play a key role in fibrosis and cirrhosis. Robust animal models of liver fibrosis and cirrhosis, as well as the recently identified critical cellular and molecular factors involved in the development of liver fibrosis and cirrhosis will facilitate the development of more effective therapeutic approaches for these conditions.

Pathogenesis of liver cirrhosis.

Wound healing requires a fine balance between the positive and deleterious effects of reactive oxygen species (ROS); a group of extremely potent molecules, rate limiting in successful tissue regeneration. A balanced ROS response will debride and disinfect a tissue and stimulate healthy tissue turnover; suppressed ROS will result in infection and an elevation in ROS will destroy otherwise healthy stromal tissue. Understanding and anticipating the ROS niche within a tissue will greatly enhance the potential to exogenously augment and manipulate healing. Tissue engineering solutions to augment successful healing and remodelling of wounded or diseased tissue rely on a controlled balance between the constructive and destructive capacity of the leukocyte secretome, including ROS. This review comprehensively considers leukocyte derived ROS in tissue repair with particular interest in surgical intervention with inclusion of a biomaterial. The article considers ROS fundamental chemistry, formation, stimulation and clearance before applying this to discuss the implications of ROS in healing tissue with and without a biomaterial. We also systematically discuss ROS in leukocyte signalling and compare and contrast experimental means of measuring ROS.

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Reactive oxygen species (ROS)--a family of fate deciding molecules pivotal in constructive inflammation and wound healing.

The Transforming Growth Factor-beta (TGF-β) family plays relevant roles in the regulation of different cellular processes that are essential for tissue and organ homeostasis. In the case of the liver, TGF-β signaling participates in different stages of disease progression, from initial liver injury toward fibrosis, cirrhosis and cancer. When a chronic injury takes place, mobilization of lymphocytes and other inflammatory cells occur, thus setting the stage for persistence of an inflammatory response. Macrophages produce profibrotic mediators, among them, TGF-β, which is responsible for activation -transdifferentiation- of quiescent hepatic stellate cells (HSC) to a myofibroblast (MFB) phenotype. MFBs are the principal source of extracellular matrix protein (ECM) accumulation and prominent mediators of fibrogenesis. TGF-β also mediates an epithelial-mesenchymal transition (EMT) process in hepatocytes that may contribute, directly or indirectly, to increase the MFB population. In hepatocarcinogenesis, TGF-β plays a dual role, behaving as a suppressor factor at early stages, but contributing to later tumor progression, once cells escape from its cytostatic effects. As part of its potential pro-tumorigenic actions, TGF-β induces EMT in liver tumor cells, which increases its pro-migratory and invasive potential. In parallel, TGF-β also induces changes in tumor cell plasticity, conferring properties of a migratory tumor initiating cell (TIC). The main aim of this review is to shed light about the pleiotropic actions of TGF-β that explain its effects on the different liver cell populations. The cross-talk with other signaling pathways that contribute to TGF-β effects, in particular the Epidermal Growth Factor Receptor (EGFR), will be presented. Finally, we will discuss the rationale for targeting the TGF-β pathway in liver pathologies.

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Transforming Growth Factor-β-Induced Cell Plasticity in Liver Fibrosis and Hepatocarcinogenesis.

Characteristics of Pyogenic Liver Abscess Patients With and Without Diabetes Mellitus

α-Lipoic acid inhibits liver fibrosis through the attenuation of ROS-triggered signaling in hepatic stellate cells activated by PDGF and TGF-β

Background Monitoring unscheduled return visits to the Emergency Department (ED) is useful to identify medical errors. Objective To investigate the differences between unscheduled return visit admissions (URVA) and unscheduled return visit no admissions (URVNA) after ED discharge. Methods From January 1, 2008 to March 31, 2008, URVA and URVNA patients who returned within 3 days after ED discharge were enrolled in the study. We compared the clinical characteristics, underlying diseases, ED crowding indicators, staff experience at the patient's first visit, and several other risk factors. We used multivariate logistic regression to evaluate differences between the two groups and to identify predictors of admission from unscheduled return visits. Results The unscheduled return visit rate was 3.1%. Of the 413 patients included, 147 patients (36%) were admitted, and had a mortality rate of 4.1%. The most common reason for the return visit was an illness-based factor (47.9%). Compared to URVNA patients, unscheduled return visit admissions had higher prevalence rates for old age, non-ambulatory status, high-grade triage, and underlying diseases (e.g., malignancy, diabetes mellitus, hypertension, coronary artery disease, heart failure, and chronic obstructive pulmonary disease). The independent predictors for URVA were: age ≥ 65 years (adjusted odds ratio [OR] 2.2, 95% confidence interval [CI] 1.4–3.5); high-grade triage (adjusted OR 2.1, 95% CI 1.3–3.2); and doctor-based factors (adjusted OR 3.5, 95% CI 2.0–6.1). More advanced staff experience (p = 0.490) and ED crowding were not significant predictors (p = 0.498 for whole-day number of patients, p = 0.095 for whole-shift number of patients). Conclusion Old age, high-grade triage, and doctor-based factors were found to be significant predictors for URVA, whereas advanced staff experience and ED crowding were not.

Unscheduled return visits with and without admission post emergency department discharge.

Probiotics modulate immunity and inhibit colon carcinogenesis in experimental models, but these effects largely depend on the bacterial strain, and the precise mechanisms are not well understood. Therefore, we studied the effect of Bifidobacterium longum and/or Lactobacillus gasseri on the development of 1,2-dimethylhydrazine (DMH)-induced colonic precancerous lesions and tumors in mice while delineating the possible mechanisms involved. The results suggest that dietary consumption of probiotics (B. longum and L. gasseri) resulted in a significant inhibition of DMH-induced aberrant crypt foci (ACF) formation in male ICR mice. Long-term (24 weeks) dietary consumption of probiotics resulted in a reduction of colon tumor multiplicity and the size of the tumors. Administration of B. longum and L. gasseri suppressed the rate of colonic mucosa cellular proliferation in a manner correlating with the inhibition of tumor induction by DMH. In addition, the phagocytic activity of peritoneal macrophages was significantly increased in the DMH-treated mice that were fed various doses of B. longum, but not with L. gasseri or combined probiotics (B. longum + L. gasseri). We also found that L. gasseri significantly increased the proliferation of RAW264.7 macrophage cells through an increase in S phase DNA synthesis, which was related to the up-regulation of proliferating cell nuclear antigen (PCNA) and cyclin A. Taken together, these results demonstrate the in vivo chemopreventive efficacy and the immune stimulating mechanisms of dietary probiotics against DMH-induced colonic tumorigenesis.

Probiotics prevent the development of 1,2-dimethylhydrazine (DMH)-induced colonic tumorigenesis through suppressed colonic mucosa cellular proliferation and increased stimulation of macrophages.

Acute onset of hemiparesis is a common initial presentation of cerebral vascular accidents, but many differential diagnoses should be considered. Hemiparesis results from an upper motor neuron lesion above the midcervical spinal cord, and the absence of cranial nerve signs or facial palsy suggests a lesion in the high cervical spinal cord. Most spinal cord lesions, however, result in quadriparesis or paraparesis, but not hemiparesis. We present a rare case of acute spontaneous cervical spinal epidural hematoma, with initial presentation of right hemiparesis and mild neck pain.

Ning Ping Foo

Papers

Characteristics of Pyogenic Liver Abscess Patients With and Without Diabetes Mellitus

α-Lipoic acid inhibits liver fibrosis through the attenuation of ROS-triggered signaling in hepatic stellate cells activated by PDGF and TGF-β

Unscheduled return visits with and without admission post emergency department discharge.

Probiotics prevent the development of 1,2-dimethylhydrazine (DMH)-induced colonic tumorigenesis through suppressed colonic mucosa cellular proliferation and increased stimulation of macrophages.

Acute spontaneous cervical spinal epidural hematoma with hemiparesis as the initial presentation